NCM 116 – LECTURE

Care of Clients with Problems in Nutrition and Gastro-intestinal metabolism

and Endocrine Function, Perception and Coordination-Acute and Chronic – lecture

MIDTERMS

CARE OF CLIENT WITH EXTERNAL BRAIN STRUCTURES

NEUROLOGIC PROBLEMS

The Human Brain

CEREBRUM
• The largest portion of the brain is the cerebrum. It
consists of two hemispheres that are connected
together at the corpus callosum.
• The cerebrum is often divided into five lobes that
are responsible for different brain functions.

Major Division of the Nervous System

A. CENTRAL NERVOUS SYSTEM (CNS),
consisting of the brain and spinal cord,
B. PERIPHERAL NERVOUS SYSTEM (PNS), the
vast network of spinal and cranial nerves linking
the body to the brain and spinal cord.
• The PNS is subdivided into:
o AUTONOMIC NERVOUS
SYSTEM
Involuntary control of:

§ Internal organs
§ Blood vessels
§ Smooth and cardiac
muscles LOBES OF THE CEREBRUM
a. SYMPATHETIC
NERVOUS SYSTEM
b. PARASYMPATHETIC
NERVOUS SYSTEM
o SOMATIC NERVOUS SYSTEM
Voluntary control of:
§ Skin
§ Bones
§ Joints
§ Skeletal muscles

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FRONTAL LOBE THALAMUS

The frontal lobe is the area of the brain responsible for • Thalamus means “inner room” in
higher cognitive functions. These includes: Greek, as it sits deep in the brain at
• Problem solving the top of the brainstem.
• Spontaneity • The thalamus is called the gateway
• Memory to the cerebral cortex, as nearly all
• Language sensory inputs pass
• Motivation through it to the
• Judgment higher levels of
• Impulse control the brain.
• Social and sexual behavior.

TEMPORAL LOBE
• The temporal lobe plays a role in HYPOTHALAMUS
emotions, and is also The hypothalamus sits under the thalamus at the top of the
responsible for smelling, brainstem. It controls many critical bodily functions:
tasting, perception, • Controls autonomic
memory, understanding nervous system
music, aggressiveness, and • Center for emotional
sexual behavior. response and behavior
• The temporal lobe also contains the • Regulates body
language area of the brain. temperature
• Regulates food intake
PARIETAL LOBE • Regulates water balance
• The parietal lobe plays a role in and thirst
our sensations of touch, • Controls sleep-wake cycles
smell, and taste. It also • Controls endocrine system
processes sensory and The hypothalamus is shaded blue. The pituitary gland
spatial awareness, and is a extends from the hypothalamus.
key component in eye-hand
coordination and arm movement. BRAIN STEM
• The parietal lobe also contains a (Extension of the Spinal Cord)
specialized area called Wernicke’s area that is A. Medulla Oblongata
responsible for matching written words with the • Contains Cardiac, Respiratory, Vomiting,
sound of spoken speech. and Vasomotor centers (heart rate,
respiration, blood vessel diameter, sneezing,
OCCIPITAL LOBE vomiting, swallowing, coughing)
• The occipital lobe is at the rear B. Pons
of the brain and controls • Respiratory center
vision and recognition. C. Midbrain
• Responsible for motor coordination
• Contains the visual reflex and auditory relay
centers

STRUCTURES PROTECTING THE BRAIN

LIMBIC LOBE
MENINGES
• The limbic lobe is located
deep in the brain, and • Covers the brain
makes up the limbic • Provides protection, support, and nourishment to
system. the brain and spinal cord.

LAYERS:
1. Dura Mater
2. Arachnoid – Contains the choroid plexus (CSF
LIMBIC SYSTEM Production
• The limbic system is the area of 3. Pia Mater
the brain that regulates
emotion and memory.
• It directly connects the lower
and higher brain functions.

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• All substances entering the CSF must filter through

these barriers
• Dyes, medications and anitibiotics are examples of
substances that cannot reach the CNS

BRAIN FUNCTIONS
VISION

• The visual cortex resides in the

occipital lobe of the brain.
• Sensory impulses travel
from the eyes via the optic
CEREBRO SPINAL FLUID nerve to the visual cortex.
• A clear and colorless fluid produced in the choroid • Damage to the visual cortex
plexus at the lateral 3rd and 4th ventricles. can result in blindness.
• Contains minimal WBC and no RBC
TASTE
• The gustatory complex (green
circle) is the part of the
sensory cortex (purple area)
that is responsible for taste.

COGNITION
• The prefrontal cortex is involved
with intellect, complex
learning, and personality.
• Injuries to the front lobe can
CSF Circulation / Pathway cause mental and personality
• Is produced in changes.
the choroid
plexus (approx. EMOTION
50 – 70%) and
• Emotions are an extremely
the remainder is
complex brain function. The
formed around
emotional core of the brain is
blood vessels
the limbic system.
and along
ventricular • This is where senses and
walls. awareness are first processed in
the brain.
• It circulates
• Mood and personality are mediated
from the lateral
through the prefrontal cortex. This part of the brain
ventricles to
is the center of higher cognitive and emotional
the foramen of
functions.
Monro
• Third Ventricle, • YELLOW: PREFRONTAL CORTEX
aqueduct of • PURPLE: LIMBIC SYSTEM
Sylvius
(Cerebral SPEECH
aqueduct), Fourth ventricle, foramen of magendie • Broca’s area is where we formulate speech and the
(Median aperture) and foramina of luschka (lateral area of the brain that sends motor
apertures) instructions to the motor cortex
• Subarachnoid Space over the rbain and spinal cord. • Injury to Broca’s area can cause
CSF is reabsorbed into venous sinus blood via difficulty in speaking. The
arachnoid granulations. individual may know what words
he or she wishes to speak, but will be
BLOOD – BRAIN BARRIER unable to do so.
• Formed by the endothelial cells of the brain • PINK: BROCA’S AREA
capillaries

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LANGUAGE NEUROTRANSMITTERS
• Wernicke’s area is a
specialized portion of
the parietal lobe that
recognizes and
understands written and
spoken language.
• Wernicke’s area
surrounds the auditory
association area
• Damage to this part of the brain can result in
someone hearing speech, but not understanding it.

HEARING
There are two auditory areas of the brain:
• The primary auditory area
(brown circle) is what
detects sounds that are
transmitted from the ear. It
is located in the sensory NEURAL COMMUNICATION
cortex SYNAPSE (SIN – aps)
• The auditory association area • Junction between the axon tip of the sending
(purple circle) is the part of the brain neuron and the dendrite or cell body of the
that is used to recognize the sounds as speech, receiving neuron
music, or noise. • Tiny gap at this junction is called the synaptic gap
or cleft
MOTOR CORTEX
• The light red area is the pre-motor NEUROTRANSMITTERS
cortex, which is responsible for • Chemical messengers that traverse the synaptic
repetitive motions of learned gaps between neurons
motor skills. The dark red • When released by the sending neuron, neuro-
area is the primary motor area, transmitters travel across the synapse and bind to
and is responsible for control of receptor sites on the receiving neuron, thereby
skeletal muscles. influencing whether it will generate a neural
• Injury to the motor cortex can result in impulse
motor disturbance in the associated body part.
NEUROTRANSMITTER
SENSORY CORTEX
• There are approximately 50 neurotransmitters
• Injury to the sensory cortex can identified
result in sensory disturbance in • Are chemicals located and released in the brain to
the associated body part. allow an impulse from one nerve cell to pass to
another nerve cell.
• Nerve cells communicate messages by secreting
neurotransmitters.
• Neurotransmitters can excite or inhibit neurons

CRANIAL NERVES

CRANIAL NERVES
Are composed of twelve pairs of nerves that emanate from
the nervous tissue of the brain.
NERVES in ORDER MODALITY FUNCTION
I. Olfactory Special Smell
Sensory
II. Optic Special Vision
Sensory
III. Oculomotor Somatic Levator
Motor palpebrae,
superioris,
superior, medial
& inferior

recti muscles
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Sensory from
pharynx, larynx
Parasympathetic Visceral & viscera
Visceral to ciliary & Sensory
Motor pupillary Sensory from
constrictor external ear
muscles Special
IV. Trochlear Somatic Superior oblique Sensory
muscle XI. Accessory Branchial Trapezius &
V. Trigeminal Branchial Muscles of nerve / Spinal Motor Sternocleidomast
Motor mastication Accessory oid muscles
XII. Hypoglossal Somatic Tongue muscles
General Sensory for Motor except
Sensory head/neck, palatoglossal
sinuses,
meninges, &
external surface CRANIAL NERVES LOCATION
of tympanic
membrane
VI. Abducens Somatic Lateral rectus
Motor muscles
VII. Facial Branchial Muscles of facial
Motor Expression

Parasympathetic
Visceral to all glands of
Motor head except the
parotid

Sensory for ear

General and tympanic
Sensory membrane

Taste anterior
Special two – thirds of
Sensory tongue
VIII. Vestibocochle Special Hearing and
ar / Auditory sensory balance
Nerve
IX. Glossopharyn Brachial Stylopharyngeus
geal motor muscles

Visceral Parotid gland

motor

Visceral Carotid body

sensory

General Sensation
sensory posterior one
third tongue &
internal surface
of tympanic
membrane

Special Taste posterior

sensory one – third
tongue
X. Vagal Brachial Muscles pharynx
Motor & larynx

Parasympathetic
to neck, thorax,
Visceral & abdomen
Motor

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Post Lumbar Tap Complications

• Post Lumbar Puncture Headache
• Temporary voiding problems
• Slight elevation of temperature
• Backache or spasms
• Stiff neck
• Rare but serious: herniation of spinal intracranial
contents, spinal epidural abscess, meningitis

Radiographic
1. Skull and Spinal Radiography
• X-ray of the skull reveal the size and shape of
the skull bones, suture separation in infants,
fracture or bony defects, erosion
or calcification
2. Ct scan
NEURODIAGNOSTIC STUDIES • Images provide cross-sectional view of the
brain, distinguish differences in tissue densities
1. Lumbar Puncture/Spinal Tap- for CSF analysis of the skull, cortex, sub cortical structures and
• CSF should be clear and colorless ventricles
• Obtained for cell count, culture, glucose and • Image is displayed on an oscilloscope or TV
protein testing monitor and is photographed digitally
• Also used to measure CSF fluid or pressure, or • Performed FIRST without contrast before
instill air, dye or meds imaging with contrast
• A spinal needle is inserted into the
subarachnoid space between 3rd and 4th or CT SCAN NURSING INTERVENTIONS
4th and 5th lumbar vertebrae • Patient needs to lie still during the entire
procedure; essential to be instructed to
Nursing Management in Assisting with Spinal Tap / patient
Lumbar Procedure • Teach relaxation techniques
Pre Procedure • Sedation maybe necessary if patient is
• Signed consent confused, agitated or restless
• Explain procedure and clarify misconceptions • Will require monitoring all through out

During the Procedure If a contrast agent/dye will be used:

• Position: Back of patient towards MD, lateral
recumbent have client draw knees to abdomen and
• Assess allergy to iodine/shellfish
chin to chest
• 4hour fasting is required prior to test
• Pillows on patient’s head and between legs
• Monitor post procedure dye reaction such
• Maintain position to prevent trauma resulting to a
as vomiting, nausea, flushing
bloody tap
• Instruct patient to breathe normally and relax; • Assess dye injection site for bleeding or
hyperventilation may lower an elevated pressure hematoma, and monitor presence of distal
altering accurate pressure reading pulses
• Assist in cleansing lumbar area • Provide fluid replacement because diuresis
with betadine sol’n and draping (observe from dye is expected
strict aseptic technique)
• MD will inject a local anesthetic to
numb puncture site 3. Magnetic Resonance Imaging
• A specimen is collected usually in 3 tubes; MUST • Uses magnetic field to create an image
be labeled in order of collection. Pressure reading • Provides info about chemical changes
may also be obtained. w/in the cell to monitor an organ’s
response to treatment
Post Procedure • Maybe used with or without dye
• Patient must lie PRONE for 2-3 hours to reduce
leakage of CSF
MRI NURSING INTERVENTIONS
• Monitor for complications of Lumbar tap
• Assess patient for claustrophobia
• Force fluid intake to prevent post-procedure
headache • Patient instructions: relaxation
technique; microphone is provided
• Monitor intake and output
inside the scanner so patient may
speak to staff
• All metal objects, credit cards, med
patches with metal/foil backing
(causes burns) must be removed

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• No metal objects, such as o2 tanks, • Place ice on the puncture site as prescribed
maybe brought inside
Surgical Intervention
4. Cerebral Angiogram Craniotomy
• Injection of contrast through the femoral • A surgical procedure that involves an incision
artery into carotid arteries to visualize through the cranium to remove accumulated blood
arteries and assess for lesions or a tumor
• Used to investigate vascular disease, Complications:
aneurysms • Increased ICP from cerebral edema
• Frequently performed before craniotomy • Hemorrhage
to assess patency and adequacy of cerebral • obstruction of the normal flow of CSF
circulation
• May use brachial artery to inject dye or a Preoperative Intervention
direct puncture of carotid or vertebral • Explain procedure to client and family
artery alternatively • Ensure informed consent has been obtained
• Make sure Pre Operative Clearance is OK as per
Angiography Nursing Intervention doctor’s order
Pre procedure • Prepare to shave clients head as prescribed
• Signed consent
• 4-6hours NPO Postoperative Intervention
• Obtain baseline neuro assessment • Monitor v/s and neuro status q 30mins- 1 hr
• Patient must be well hydrated 2days • Monitor increased ICP
prior to the exam. Patient will be asked to • Monitor for decreased LOC, motor weakness or
void before going to the x-ray department paralysis, aphasia, visual changes and personality
• Explain procedure to patient. changes
• Patient has to be immobile during the • Maintain mech vent and slight hyperventilation for
entire procedure. the first 48hrs to prevent increase in ICP as per
• A brief feeling of warmth in the face, doctor’s order
behind the eyes, or the jaw, teeth, tongue, • Stabilize client before surgery
lips will be felt. • Avoid neck or hip flexion and maintain head in
• A metallic taste after the injection of the midline neutral position
contrast agent will be experienced. • Provide quiet environment
• Mark peripheral pulses • Monitor head dressing frequently for signs
of drainage
During Procedure • Mark areas of drainage at least once/shift
• The groin will be shaved and prepared, • If on ventriculostomy maintain suction
injected with a local anesthetic to numb as of drain, record amount and color; notify MD
catheter is inserted
if drainage is greater than 30-50ml
• Catheter will be flushed
• Record strict measurement of I&O hourly
with heparinized saline
• Monitor electrolyte values
Post Procedure
• Apply ice pack or cool compresses as prescribed
• Observe for signs of altered cerebral
for periorbital edema and ecchymosis
blood flow due to minor or major arterial
blockage caused by thrombosis, embolism Positioning of Patient after Craniotomy
or hemorrhage producing neurologic
• varies
deficits such as:
• Incorrect positioning may cause serious and
possibly fatal complications
a) Altered level of responsiveness
and consciousness
A. Infratentorial Surgery (cerebellum)
b) Hemiparesis
c) Speech disturbances
• Flat position without head elevation or may order
head of bed at 40-35 degrees
• Monitor Neuro status and V/S until stable
• Do not elevate the head in the acute phase of care
• Monitor for swelling in the neck and for
after surgery w/o MD order
dysphagia and NOTIFY MD if these occur
• Maintain bed rest for 12hrs as prescribed
• Elevate head of bed 15-30 degrees only B. Supratentorial Surgery (cerebrum)
if prescribed
• Keep bed flat if femoral artery is used, • Head of bed elevation 30 degrees to promote
as prescribed venous outflow through the jugular vein
• Assess peripheral pulses • Do not lower head of bed w/o MDs order
• Apply sandbag and pressure dressing to
the injection site as prescribed

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COMMON NEUROLOGIC • Muscle contraction in the neck and scalp is

MANIFESTATIONS common, with associated muscle ache and
HEADACHE localized tenderness, exhaustion, and mood
• (cephalgia) changes.
• is one of the most common of all human physical • Any physical exertion exacerbates the headache
complaints. pain.
• symptom rather than a disease entity • During this post headache phase, patients may
• it may indicate organic disease (neurologic or other sleep for extended periods.
disease), a stress response, vasodilation (migraine),
skeletal muscle tension (tension headache), or a TENSION HEADACHE
combination of factors • Is characterized by a steady, constant feeling of
pressure that usually begins in the forehead,
PRIMARY HEADACHE temple, or back of the neck.
• Include migraine, tension-type, and cluster • It is often bandlike or may be described as “a
headaches weight on top of my head.”
• Migraine • Tend to be more chronic than severe and are
o is a symptom complex characterized by probably the most common type of headache
periodic and recurrent attacks of severe
headache. CLUSTER HEADACHE
o Caused by primarily a • Severe form of vascular headache.
vascular disturbance that occurs • Are unilateral and come in clusters of one to eight
more commonly in women and has daily, with excruciating pain localized to the eye
a strong familial tendency. and orbit and radiating to the facial and temporal
regions.
CLINICAL MANIFESTATION • The pain is accompanied by watering of the eye
MIGRAINE and nasal congestion.
• The migraine with aura can be divided into four • Each attack lasts 30 to 90 minutes and may have a
phases: prodrome, aura, the headache, and recovery crescendo–decrescendo pattern
(headache termination and postdrome).
• Often described as penetrating and steady
• They are seen five times more frequently in men
1. Prodrome
than women.
• Symptoms include depression, irritability, feeling
cold, food cravings, anorexia, change in activity
SECONDARY HEADACHE
level, increased urination, diarrhea, or
constipation. • Associated with an organic cause, such as a brain
• Occur hours to days before a migraine headache. tumor or an aneurysm.
• Serious disorders related to headache include brain
2. Aura Phase tumors, subarachnoid hemorrhage, stroke, severe
• Characterized by focal neurologic symptoms, hypertension, meningitis, and head injuries.
visual disturbances (ie, light flashes and bright
spots) are common and may be hemianopic Medical Management Nursing Management
(affecting only half of the visual field).
Triptans Relieving pain
• Other symptoms that may follow include numbness
and tingling of the lips, face, or hands; mild
• Serotonin receptor • Comfort measures
confusion; slight weakness of an extremity;
drowsiness; and dizziness.
agonists, antimigraine • Application of local heat
agents or massage.
• Usually lasts less than an hour and may provide
• Cause vasoconstriction, • Additional strategies may
enough time for the patient to take the prescribed
reduce inflammation, include the use of
medication to avert a full-blown attack
and may reduce pain analgesic agents,
transmission. antidepressant
3. Headache Phase.
medications, and muscle
• As vasodilation and a decline in serotonin levels
The five triptans in routine relaxants as prescribed.
occur, a throbbing headache intensifies over several
clinical use include • Encourage relaxation
hours.
• Sumatriptan (Imitrex) techniques such as dbe,
• This headache is severe and incapacitating and is
• Naratriptan (Amerge) guided imagery and etc.
often associated with photophobia, nausea, and
vomiting. • Rizatriptan (Maxalt)
• Zolmitriptan (Zomig)
• Its duration varies, ranging from 4 to 72 hours.
• Almotriptan
4. Recovery Phase
• In the recovery phase (termination and postdrome),
the pain gradually subsides.

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INCREASED INTRACANIAL PRESSURE • Pregestational IDDM

• The rigid cranial vault contains brain tissue (1,400 • Maternal hyperthermia
g), blood (75 mL), and CSF (75 ml) • Genetics
• The volume and pressure of these three • Amniotic band disruption sequence
components are usually in a state of equilibrium • Teratogens
and produce the ICP • Radiation
• ICP is usually measured in the lateral ventricles
• It can result from head injury, brain tumor, RISK FACTOR
hydrocephaly, meningitis, encephalitis, or • Maternal malnutrition
intracerebral hemorrhage. • Drug exposure
• Increased ICP should be treated as a medical • Low socioeconomic group
emergency • Older maternal age
MANIFESTATION OF INCREASED ICP DIAGNOSTICS
• Headache • Amniocentesis (to det increased levels of alpha-
• Change in level of consciousness fetoprotein
• Irritability • Alpha-fetoprotein level – increase suggests a NTD)
• Increased systolic BP • Urine estriol level
• Decreased HR (early) • Pre-pregnancy serum folic acid
• Increased HR (late) • Fetal ultrasound
• Decreased RR • MRI
• Hemiparesis • CT scan
• Loss of oculomotor control
• Photophobia (light sensitivity) TYPES
• Vomiting (with subsequent decreased headache) A. Anencephaly
• Diplopia (double vision) • large skull defect with no cortex. many are stillborn
• NOTE: BLAP and other die within days of birth
MANAGEMENT OF INCREASED ICP
1. Elevate head of bed 15 to 30 degrees. Keep head in
neutral alignment. Do not flex or rotate neck.
2. Establish IV access.
3. Insert Foley catheter as per doctor’s order.
4. Meds that may be used include osmotic diuretics,
sedatives, neuromuscular blocking agents,
corticosteroids, and anticonvulsants.
5. Restrict fluids follow the doctor’s fluid regimen.
6. Closely monitor vital signs and perform neuro
checks.
7. Monitor fluids and electrolytes
8. Schedule all procedures (including bathing and
especially suctioning) to coincide with periods of
sedation.
9. Discourage patient activities that result in use of
Valsalva’s maneuver.
10. Keep environment as quiet as possible. B. Encephalocele
11. Ventilator may be used to maintain PaCO2 • Projections of cranial content through a bony skull
between 35-45. defects, usually occipital region.

NEUROLOGICAL DYSFUNCTION
NEURAL TUBE DEFECTS
• Neural tube defects (NTDs) are one of the most
common birth defects, occurring in approximately
one in 1,000 live births in the United States.
• An NTD is an opening in the spinal cord or brain
that occurs very early in human development

ETIOLOGY
• It is UNKNOWN, only associated with the
following
• Inadequate folic acid
• Medications – antimetabolites of folic acid,
anticonvulsant
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c) Spina Bifida w/ Meningomyelocele

• Defect of vertebral arches with protrusion of
meninges, spinal cord, CSF, nerve roots.

C. Spina Bifida CLINICAL MANIFESTATION

• CNS defect that occurs as a result of incomplete • Depends on the spinal cord involvement
closure of one or more vertebrae. • Visible spinal defect
• Flaccid paralysis of the legs
• Altered bladder and bowel function
• Hip and joint deformities

CEREBRAL PALSY
• Non progressive disorder of movement and posture
that results from lesion of the immature brain.

RISK FACTOR
• Prematurity
• Birth asphyxia
• Early infection or trauma

TYPES OF CEREBRAL PALSY

Types of SPINA BIFIDA

a) Spina Bifida Occulta:
• Defect in the vertebral arches without herniation of
any spinal content.
• Birthmarks, dimples, or hairy tuft at the base of the
back.

CLINICAL MANIFESTATION
• Tones remains relatively constant regardless of
b) Spina Bifida w/ Meningocele activity and level of arousal
• Defects in vertebral arches with protrusion of • Significant Hyperreflexia
meninges • Stiff and rigid arms or legs
• Persistence of Primitive and pathologic reflexes
• Extreme irritability and crying
• Feeding difficulties
• Delayed gross development
• Opisthotonos posture

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MANAGEMENT is more likely to trigger symptoms of Reye's

• Multidisciplinary approach syndrome. A screening test can determine if your
• Therapeutic goal includes minimizing impairments, child has a fatty acid oxidation disorder.
maximizing function, preserving general health
• Therapies: CDC DIAGNOSTIC CRITERIA FOR REYE’S SYNDROME
o Speech, physical, occupational Acute noninflammatory encephalopathy with an altered level
o Botulinum toxin a: botox of consciousness.
o Massage Hepatic dysfunction with a lover biopsy showing fatty
• Prosthetics/Orthotics metamorphosis or a more than 3 – fold increase in alanine
• Surgery aminotransferase (ALT), aspartate aminotransferase (AST),
• Hyperbaric Oxygen and/or ammonia levels.
No other explanation for cerebral edema or hepatic
NOTE: abnormality.
*** Injecting botulinum toxin type-A would result in Cerebral Spinal Fluid (CSF) with white blood cells (WBC)
decreased muscle activity by blocking the release of 8/mm3 or fewer.
acetylcholine from the neuron Brain biopsy showing cerebral edema without inflammation.
*** hyperbaric oxygen therapy (HBOT), is the medical use
of oxygen at a level higher than atmospheric pressure TREATMENT
• No specific treatment
NURSING MANAGEMENT • Supportive care
• Assess child’s developmental level and intelligence • 10% dextrose,
• Encourage early intervention and participation in • Blood transfusion
school programs • intubation may be necessary to provide adequate
• Prepare for using mobilizing devices to prevent oxygenation
deformities • Intracranial pressure must be monitored and
• Communicate with the child on a functional level, controlled in patients with cerebral edema.
not on chronological age level • Management of cerebral edema may involve fluid
• Provide safe environment restriction, diuresis, and corticosteroids.
• Provide safe, appropriate toys for age and Pentobarbital has been given to patients to decrease
developmental level cerebral metabolic demands.23 Therapies to reduce
• Position upright after meals hyperammonemia may also be indicated. In
patients who develop seizures, antiepileptic
REYE’S SYNDROME medications may be necessary.
• also known as Reye syndrome, is a rare but serious
condition that causes swelling in the liver and MULTIPLE SCLEROSIS
brain. • Immune-mediated progressive demyelinating
• Reye's syndrome can occur at any age but usually (myelin sheath of neurons is damaged) disease
affects children and teenagers after a viral of the CNS
infection, most commonly the flu or chickenpox. • A chronic degenerative progressive disease of the
CNS
REYE’S SYNDROME CLINICAL STAGING SYSTEM • Characterized by small patches of demyelination in
MILD – MODERATE the brain & spinal cord.
STAGE 1 Vomiting, Laboratory evidence of liver • Aka: disseminated sclerosis
dysfunction, lethargic, sleepy.
STAGE 2 Deeply lethargic, restless, confused, delirious, EPIDMIOLOGY
combative, hyperventilation, hyperreflexia • Major cause of chronic disability in young adults
STAGE 3 Obtunded or in a light coma, decorticate rigidity • Onset of symptoms usually occurs between 20 and
SEVERE 40.
STAGE 4 Deepening coma, seizures, decerebrate rigidity, • Occurs more frequently in Caucasian females than
fixed pupils, loss of oculovestibular reflexes. males
STAGE 5 Seizures, deep coma, flaccid paralysis, absent
deep tendon reflexes, respiratory arrest, and ETIOLOGY
fixed, dilated pupils • Cause is not known
• The use of aspirin during a viral illness has most • Current theories identify autoimmune- mediated
commonly been linked to Reye's syndrome. inflammatory demyelination and axonal injury
• Medium-chain acyl-CoA dehydrogenase (MCAD) • Multiple factors are involved (research)
deficiency. MCAD deficiency is a fatty acid
oxidation disorder. Fatty acid oxidation disorders
are a group of inherited metabolic disorders in
which the body is unable to break down fatty acids.
This happens because an enzyme is missing or not
working properly. In people with a fatty acid
oxidation disorder, aspirin use during a viral illness

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PATHOPHYSIOLOGY DIAGNOSTIC METHODS

A. MRI
• To visualize small plaques, evaluate cause and
effects of treatment.
B. Electrophoresis
• Used to study the CSF, abnormal IgG appears
in the CSF
• A technique widely used to separate and
identify serum proteins and other substances
up to 95% of patient.
C. Fluid – Attenuated – Inversion – Recovery (FLAIR)
• Able to detect two or three times the number
of lesions seen in MRI
D. Magnetic Resonance Spectroscopy
• Decreased level of N – Acetylaspartate (NAA)
suggest presence of axonal damage
• N – Acetylaspartate – is the second most
concentrated molecule in the brain after the
amino acid glutamate.

MEDICAL MANAGEMENT
1. Immunomodulating Drugs - slows disease
progression, reduces relapse
o E.g. Interferon beta-1a (Avonex)
2. Immunosuppresant Drugs – same as #1
o E.g. Mitoxantrone ( Novantrone)
3. Corticosteroid Drugs - exacerbations
o E.g. Corticotropin (ACTH), Prednisone
Deltasone
4. Muscle Relaxants - spasticity
o E.g. Diazepam (Valium), Baclofen
(Lioresal)
5. Antiepileptic Drugs – neuropathic pain
o eg. Carbamazepine (Tegretol)
CLINICAL FINDINGS 6. Anti-depressants - depression
o e.g. Amitriptyline (Elavil)
7. Stimulant Drugs - fatigue
o e.g. Amantadine (Symmetrel)
8. Cholinergic - urinary retention
o e.g Neostigmine (Prostigmin)
9. Anti - cholinergic - urinary frequency
o e.g. Probantin (Pro - Banthine)

SURGICAL MANAGEMENT

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NURSING MANAGEMENT SURGICAL MANAGEMENT

• Evaluate sac and measure lesion Microvascular Decompression of the Trigeminal Nerve.
• Perform neurological assessment • Intracranial approach used to decompress the
• Monitor increase in ICP trigeminal nerve by relieving the contact between
• Protect sac, using aseptic technique the cerebral vessel and trigeminal nerve root entry.
• Place in prone position, head turned to one side for • Relieves facial pain while preserving normal
feeding sensation, but it is a major procedure, involving a
• Assess for early signs of infection craniotomy.
• Administer medication as ordered (antibiotics)
Percutaneous Radiofrequency Thermal Coagulation
TRIGEMINAL NEURALGIA • Produces a thermal lesion on the trigeminal nerve
• (Tic douloureux) • Although pain is relief dysesthesia and loss of
corneal reflex may occur
• is a condition of the
fifth cranial nerve
characterized by Þ Percutaneous Balloon Microcompression
paroxysms of pain Þ Disrupts large myelinated fibers of all 3 branches of the
in the area trigeminal nerve
innervated by any of Þ Balloon is filed with a contrast material for fluoroscopic
the three branches identification and compresses the nerve root for 1
• Most commonly minute.
occurs in the second
and third branches NURSING MANAGEMENT
of the trigeminal Preventing Pain
nerve • Providing cotton pads and room-temperature water
for washing the face
CAUSES / RISK FACTORS • Instruct to rinse with mouthwash after eating when
tooth-brushing causes pain, and performing
• Demyelination of axons in the ganglion, root and
personal hygiene during pain-free intervals
nerve
• Instruct to take food and fluids at room
• Multiple sclerosis
temperature, to chew on the unaffected side, and to
• Swollen blood vessels or tumor
ingest soft foods.
• More common in women between 5th and - decade
of life
PROVIDING POST – OPERATIVE CARE
MANIFESTATION • Postoperative neurologic assessments
• If the surgery results in sensory deficits to the
• Pain that ends as abruptly as it starts and is
affected side of the face, the patient is instructed
described as a unilateral shooting and stabbing
not to rub the eye, because pain will not be felt if
sensation.
there is injury.
• Associated involuntary contraction of the facial
• The eye is assessed for irritation or redness.
muscles can cause sudden closing of the eye or a
• Artificial tears may be prescribed to prevent
twitch of the mouth
dryness in the affected eye.
• The patient is cautioned not to chew on the affected
FACTORS THAT TRIGGER
side until numbness has diminished.
• Paroxysms can occur with any stimulation of the • The patient is observed carefully for any difficulty
terminals of the affected nerve branches such as in eating and swallowing foods of different
washing the face, shaving, brushing the teeth, consistency.
eating, and drinking.
MYASTHENIA GRAVIS
MEDICAL MANAGEMENT
• Chronic
PHARMACOLOGIC THERAPY • Autoimmune
1. Anticonvulsant agents, such as carbamazepine • Progressive neuromuscular disease affecting the
(Tegretol)
voluntary degree of abnormal weakness and
• Relieve pain by reducing the transmission of fatigability of skeletal muscles (voluntary muscles)
impulses at certain nerve terminals.
• S/e: nausea, dizziness, drowsiness, and aplastic
anemia.
• Monitor for bone marrow depression during long
term therapy.
2. Gabapentin (Neurontin) and baclofen (Lioresal)
• Used for pain control.
3. Phenytoin (Dilantin)
• May be used as adjunctive therapy

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MANIFESTATION 2. Immunosuppressive Therapy

• decrease the amount of antibody production
SUBJECTIVE OBJECTIVE • E.g:
• Corticosteroid
• Extreme muscle • Ptosis of the eyelid
weakness • Weak voice
3. Cytotoxic Medications
• Dysphagia (dysphonia)
• Decrease the circulating anti acetylcholine receptor
• Diplopia • Myasthenic smile
• E.g:
• Dysarthria (difficulty (snarling, nasal
Cyclophosphamide (Cytoxan)
speaking) smile)
• Dyspnea • Snarling face
4. Intravenous immune globulin (IVIG)
• Strabismus • Treat exacerbation
• Weakness in intercostal
muscles resulting in 5. Therapeutic Plasma Exchange (TPE)
decreasing vital or plasmapheresis
capacity and • Used to treat exacerbations
respiratory failure
SURGICAL MANAGEMENT
ASSESSMENT & DIAGNOSTIC FINDINGS
Thymectomy
1. Acetylcholinesterase inhibitor test Administration
• Can produce antigen-
of edrophonium chloride (Tensilon) IV; 30 seconds
specific immunosuppression
after injection facial muscle weakness and ptosis
• It may take 1 year after the
should resolve for about 5 minutes. Atropine
removal before the patient
should be available
can benefit.
2. Serum Assay for Circulating anti acetylcholine
receptor (+) MG if increased
3. Ice Test for pt. with asthma or cardiac condition ice
is held over the pt. eye for 1 min. ptosis will be
resolved
4. Acetylcholine antibodies
5. Reduced response to electrical stimulation NURSING CARE
• Improving respiratory function
POTENTIAL COMPLICATIONS • Increasing physical mobility
Myasthenic Crisis • Improving communication
• Sudden onset of muscle weakness as a result of • Providing eye care
under medication or non-cholinergic medication at • Preventing aspiration
all
• Triggered by emotional upset, systemic infection, DYSFUNCTION OF THE BRAIN
medication, surgery or trauma. CEREBROVASCULAR DISORDER
Signs • Stroke is the primary cerebrovascular disorder in
o Sudden onset of acute respiratory distress
the United States and in the world.
o Inability to swallow or speak
• 2nd leading cause of death.
Cholinergic Crisis
TYPES OF CEREBOVASCULAR DISORDER
• Caused by over medication w/ anticholinesterase
Signs A. Ischemic - damage to brain due to a clogged artery
o Muscle weakness w/ respiratory B. Hemorrhagic - blood vessel burst leaking blood
depression into brain tissues
o Gi symptoms (nausea, vomiting, diarrhea,
increased salivation) MAJOR TYPES OF STROKE AND THEIR CAUSES
o Sweating, & bradycardia. CLASSIFICATION CAUSES
ISCHEMIC Large artery thrombosis
MEDICAL MANAGEMENT Small penetrating artery
thrombosis
• No cure
Cardiogenic Embolic
1. Anticholinesterase Other
HEMORRHAGIC Intracerebral hemorrhage
• Increase the relative concentration of available
Subarachnoid hemorrhage
acetylcholine at the neuro muscular junction
Cerebral Aneurysm
• E.g:
Arteriovenous
o Pyridostigmine bromide (mestinon)
Malformation
o Neostigmine bromide (prostigmin)

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MODIFIABLE NON – MODIFIABLE 5. Dysphagia

• Hypertension • Age • Difficulty in swallowing
• Hypercholesterolemia • Sex
• Atherosclerosis • Family Sensory Deficits
• Atrial fibrillation history • Paresthesia (occurs on the side opposite the
• Obesity • Past medical lesion)
• Drugs and alcohol history • Numbness and tingling of extremity
• TIA’s • Difficulty with proprioception

Verbal Deficits
1. Expressive aphasia
• Unable to form words that are understandable; may
be able to speak in single-word responses

2. Receptive aphasia
• Unable to comprehend the spoken word; can speak
but may not make sense

3. Global (mixed) aphasia

• Combination of both receptive and expressive
aphasia.

Cognitive Deficits
• Short- and long-term memory loss
• Decreased attention span
• Impaired ability to concentrate
NEUROLOGIC DEFICIT- MANIFESTATION • Poor abstract reasoning
Visual Field Deficits • Altered judgment

1. Homonymous hemianopsia (loss of half of the Emotional Deficits

visual field) • Loss of self-control
• Unaware of persons or objects on side of • Emotional lability
visual loss • Decreased tolerance to stressful situations
• Neglect of one side of the body • Depression
• Difficulty judging distances • Withdrawal
• Fear, hostility, and anger
2. Loss of peripheral vision • Feelings of isolation
• Difficulty seeing at night
• Unaware of objects or the borders of objects

3. Diplopia
• Double vision

Motor Deficits

1. Hemiparesis
• Weakness of the face, arm, and leg on the
same side (due to a lesion in the opposite
hemisphere).

2. Hemiplegia
• Paralysis of the face, arm, and leg on the same
side (due to a lesion in the opposite
hemisphere.

3. Ataxia TIME COURSE IN STROKE

• Staggering, unsteady gait TIA • Temporary episodes of
• Unable to keep feet together; needs a broad neurologic dysfunction
base to stand lasting for seconds or
minimum but not longer
4. Dysarthria than 24 hrs.
• Difficulty in forming words

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• Complete recovery occurs Other Tx measures include the following:

between attacks • Elevation of the head of the bed to promote
venous drainage and to lower increased ICP
• Intubation with an endotracheal tube to
establish a patent airway, if necessary
• Continuous hemodynamic monitoring
• Systolic pressure should be maintained at less
REVERSIBLE Consistent but more pronounce than 180 mm Hg, diastolic pressure at less than
ISCHEMIC than TIA and last more than 24 hrs 100 mm Hg to reduce the potential for
NEUROLOGIC additional bleeding or further ischemic damage
DEFICIT • Neurologic assessment.
STROKE IN Progressing stroke
EVOLUTION SURGICAL:
Carotid Endarterectomy (CEA)
COMPLETED No further progression of hypoxic • Surgical reopening of an artery obstructed by
STROKE insult ATHEROMA.
• Removal of an atherosclerotic plaque or thrombus
DIAGNOSTIC TEST from the carotid.
• Computed Tomography
• 12 lead electrocardiogram and carotid ultrasound Carotid Artery Stenting (CAS)
• Cerebral angiography • With or without angioplasty
• Transcranial Doppler flow studies • Less invasive
• MRI • Used for the treatment of carotid stenosis

MEDICAL AND SURGICAL MANAGEMENT NURSING MANAGEMENT

Meds: • Improving mobility and preventing joint deformity
• Changing positions, maintaining skin integrity
1. Thrombolytic Therapy – Recombinant t-PA • Establishing exercise program
• minimum dose is 0.9 mg/kg; the maximum • Enhancing Self care, activities of daily living
dose is 90 mg. • Managing Sensory-Perceptual Difficulties
• The loading dose is 10% of the calculated dose • Attaining bowel and bladder control
and is administered over 1 minute. • Improving thought process
• Improving communication
o The remaining dose is administered over 1 • Improving family coping
hour via an infusion pump. • Helping patient cope with sexual dysfunction
o After the infusion is completed, the line is • Continuing care
flushed with 20 mL of normal saline
solution to ensure that all the medication HEMORRHAGIC STROKE
is administered
CAUSE
Side Effects: • Intracerebral hemorrhage
• Bleeding - most common side effect of t-PA • Subarachnoid hemorrhage
administration • Cerebral aneurysm
• Arteriovenous malformation
Nursing Responsibilities:
• Cardiac monitoring CLINICAL MANAGEMENT
• Vital signs are obtained every 15 minutes for the Neurologic deficits similar to ischemic stroke plus.
first 2 hours, every 30 minutes for the next 6 hours, • Sudden, unusually severe headache
then every hour for 16 hours. • Loss of consciousness
• Blood pressure should be maintained with the • Nuchal rigidity
systolic pressure less than 180 mm Hg and the • Visual disturbances
diastolic pressure less than 100 mm Hg. • Tinnitus, dizziness
• Airway management is instituted based on the • Hemiparesis
patient’s clinical condition and arterial blood gas
values. SURGICAL AND MEDICAL MANAGEMENT
2. Anticoagulant (IV heparin or low- • Analgesics
molecularweight heparin) for ischemic strokes. • Bed rest with sedation
3. Careful maintenance of cerebral hemodynamics • Surgical Evacuation (Craniotomy)
to maintain cerebral perfusion. o If cerebellar hemorrhage diameter exceeds
4. Reduce ICP by administering an osmotic 3 cm
diuretic (eg, mannitol), maintaining PaCO2 o Glasgow Coma Scale score is below 14
within the range of 35 to 45 mm Hg, and • Aneurysm Clipping
positioning to avoid hypoxia • Craniectomy

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CRANIOTOMY PROCEDURE (F.2) Aneurysm clips come in

(F.1) Craniotomies a variety of sizes and curves.
are often named for A clip applier opens the
the bone being blades of the aneurysm clip.
removed. Some They are made of titanium,
common they stay forever.
craniotomies include
frontotemporal,
parietal, temporal,
and suboccipital. (F.3) A craniotomy is made in
the skull over the area where
(F.2) The patient’s the aneurysm is located. The
head is placed in a bone flap is lifted and
three-pin Mayfield temporarily removed.
skull clamp. The
clamp attaches to the
operative table and
holds the head
absolutely still
during delicate brain (F.4) A titanium clip is placed
surgery. The skin across the neck of an
incision is usually made behind the hairline (dashed line). aneurysm preventing blood
from entering.
(F.3) A craniotomy
is cut with a special
saw called a
craniotome. The
bone flap is NURSING MANAGEMENT
removed to reveal • Monitor for neurologic deterioration
the protective • Implement aneurysm precaution
covering of the • Monitor and manage complications:
brain called the o Vasospasm
dura. o Seizure
o Hydrocephalus
o Rebleeding
(F.4) The dura is • Teaching patient self-care
opened and folded • Continuing care.
back to expose the
brain. DYSFUNCTION OF THE PERIPHERAL NERVOUS
SYSTEM
AMYOTROPHIC LATERAL SCLEROSIS (LOU GEHRIG
DISEASE)
(F.5) The bone flap • Is a disease of unknown cause in which there is a
is replaced and loss of motor neurons (nerve cells controlling
secured to the skull muscles) in the anterior horns of the spinal cord
with tiny plates and and the motor nuclei of the lower brain stem.
screws. • Several theories exist regarding the cause of als,
including autoimmune disease and free radical
damage.
• The leading theory held by researchers is that
ANEURYSM CLIPPING overexcitation of nerve cells by
(F.1) Most the neurotransmitter glutamate leads to cell injury
aneurysms resemble and neuronal degeneration
a balloon, with a • ALS is incurable and fatal, with median survival of
narrow neck at its 3 years
origin and a large
expanding dome.
Typically, a clip is
placed across the
neck of the aneurysm
to prevent blood
from entering the
dome.

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RISK FACTOR • The voice assumes a nasal sound, and articulation

• Smoking becomes so disrupted that the speech
• Viral infections is unintelligible.
• Autoimmune disease • Some emotional lability may be present, but
• Environmental exposure to toxins intellectual function is not impaired.
• Common in male between 40-60 years old
MEDICAL MANAGEMENT
SIGNS AND SYMPTOMS • Riluzole (Rilutek), a glutamate antagonist, slows
• In 75-80% of patients, symptoms begin with limb the deterioration of motor neurons (dose of 100 mg
involvement. riluzole per day)
• Symptomatic treatment and rehabilitative measures
Initial complaints in patients with lower limb onset are are employed to support the patient and improve
often as follows: the quality of life.
• Tripping, stumbling, or awkwardness when running • Baclofen (Lioresal), dantrolene sodium (Dantrium),
• Foot drop; patients may report a "slapping" gait or diazepam (Valium) may be useful for patients
troubled by spasticity, which causes pain and
Initial complaints with upper limb onset include the interferes with self-care.
following: • A patient experiencing problems with aspiration
and swallowing may require enteral feeding.
• Reduced finger dexterity, cramping, stiffness, and
weakness or wasting of intrinsic hand muscles • Mechanical ventilation (using negative-pressure
• Wrist drop interfering with work performance. ventilators) is an option when alveolar
hypoventilation develops.
With bulbar onset symptoms 1st appear in the face or
neck (20-25%), initial complaints are as follows: BELL’S PALSY
• Slurred speech, hoarseness, or decreased volume of • Facial paralysis that occurs on one side of the face
speech as a result of inflamed 7th cranial nerve
• Aspiration or choking during a meal. • Facial neuropathy characterized by paresis and pain
• Affects men and women equally
Emotional and special cognitive difficulties in some ALS
patients are as follows: The cause is unknown, although possible causes may
• Involuntary laughing or crying include vascular ischemia, viral disease (herpes simplex,
• Depression herpes zoster), autoimmune disease, or a combination of all
• Impaired executive function of these factors
• Maladaptive social behavior
SUBJECTIVE • Facial pain
Features of more-advanced disease are as follows: • Difficulty eating
• Muscle atrophy becomes more apparent • Altered taste
• Spasticity may compromise gait and manual OBJECTIVE • Distortion of face
dexterity • Difficulty with
• Muscle cramps are common articulation
• Rarely, painful joint contractures may result from • Diminished blink
immobility reflex
• Increased lacrimation
Progression of bulbar disease leads to the following: ASSESSMENT • Presence or absence
• Voice changes: Hypernasality and development of of blink reflex &
a strained, strangled vocal quality; eventually, ability to close eye
speech may be lost • Facial pain
• Swallowing difficulties, usually starting with • Nutritional intake &
liquids. the ability to chew &
swallow
CLINICAL MANIFESTATION • extent of facial
• Fatigue paralysis
• Progressive weakness and atrophy of the muscles
of the arms, trunk, or legs, cramps, CLINICAL MANIFESTATION
• Muscle fasciculations (twitching) • Recovery 3-5 weeks
• Muscle incoordination • Prednisone Therapy
• Muscle spasticity • Analgesic agents
• Brisk and overactive deep tendon stretch reflexes • Heat, massage & electric stimulation
• difficulty talking, swallowing, and • Prevention of Corneal irritation
ultimately breathing.
• Weakness of the posterior tongue and palate
impairs the ability to laugh, cough, or even blow
the nose
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NURSING CONSIDERATION 4. Miller-Fisher variant rarest type (ataxia,

• Teach client to prevent corneal irritation by using areflexia and opthalmoplegia.
artificial tears, manually closing the eye &
applying an eye protective shield Assessment Findings Diagnostic Tests
• Teach client to keep the face warm must include
• Teach the client to massage face gently & perform Occupation Exclusion of other
simple facial exercises such as wrinkling, blowing, Infectious and symptoms
whistling exposure history ( poliomyelitis, botulism,
• Encourage ventilation of feelings because self- Extension of weakness exposure to heavy metals)
image may be affected. Location and movement and
progression of paresis History of the patient
• Support client’s nutritional status by providing
Vital signs Muscle strength tests
privacy & small, frequent feedings & encourage
Signs of Muscle activity tests
the client to favor the unaffected side while eating
decreased oxygenation Physical examination
• Avoid exposure of the face to colds
Reflex tests, such as the
knee-jerk reaction
Guillain-Barre Syndrome
Nerve conduction velocity
(Acute Idiopathic Polyneuritis) tests
• An autoimmune attack of the peripheral nerve Spinal tap, to check
myelin for higher than
• characterized by acute neuropathy involving motor expected levels of protein
and sensory nerves throughout the peripheral in the cerebrospinal fluid.
nervous system
CSF analysis

CLINICAL MANIFESTATION
• Muscle weakness
• Diminished reflexes
• Hyporeflexia
• Neuromuscular respiratory failure
• Paresthesia
• Blindness
• Bulbar muscle weakness
• Areflexia

MEDICAL MANAGEMENT
• Plasmapheresis (IVIG) - trials have proven the
effectiveness of this form of treatment.
• Support of vital function: NGT insertion,
intermittent catheterization, intubation or
ventilatory support
• Anticoagulant agent
• Steroids
• IVF therapy
• Monitor vital signs, vital capacity, breath sounds &
ABG
• Keep airway & tracheostomy set at bedside
• Suction, provide fluid replacement therapy, &
monitor functioning of the respirator as required
• Provide emotional support to the client & family
• Provide explanations of disease process & care
• Refer client & family to a support group or
foundation for additional information & resources
• Prevent complications of Immobility
• Skin care, apply anti embolic stockings
TYPES • Range of motion exercise, position changes
1. Ascending GBS Weakness in the lower • Coughing & deep breathing.
extremities which progresses upward and has
potential for respiratory failure
2. Purely motor with no altered sensation
3. Descending GBS affects the head and neck

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KCPD 20